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This review highlights zinc transporters' dysregulation in diabetes and related diseases, suggesting therapeutic avenues.
Zinc is an essential trace element that participates in a wide range of physiological processes. Cellular zinc homeostasis is tightly controlled by two families of transporters: the Zrt/Irt-like protein (ZIP/ SLC39) family, which mediates zinc influx into the cytoplasm, and the zinc transporter (ZnT/ SLC30) family, which facilitates zinc efflux or sequestration into intracellular organelles. Growing evidence implicates dysregulated expression or function of zinc transporters in the onset and progression of diverse pathological conditions. In this review, we provide a comprehensive overview of the molecular regulation and recent advances on ZIPs and ZnTs in diabetes and related disorders, including obesity, neurodegenerative diseases, cancers and immune dysregulation. We also discuss ongoing scientific controversies regarding the mechanistic roles of zinc transporters, particularly ZnT8, in the pathogenesis of diabetes. Finally, we provide perspectives on the translational potential of zinc transporter-targeted strategies in precision medicine.
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Xu et al. (2025) studied this question.
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